Alfredo L. Pauca

Augmentation of the aortic and central arterial pressure waveform.

Late systolic augmentation of the ascending aortic and central arterial pressure wave is a characteristic feature of aging, and is attributable to stiffening of the aorta and major central arteries. It is caused by increased pulse wave velocity in these vessels with early return of wave reflection from peripheral sites, predominantly in the lower part of the body. Augmentation is measurable through identification of the shoulder or early systolic peak of pressure, which corresponds to peak flow in the aorta, and measurement from this point to the second peak, or shoulder of the wave in late systole. Difficulties in measurement of augmentation arise from problems in identification of the initial shoulder, especially when this is close to the foot of the reflected wave, to amplification of the pulse wave between ascending aorta and carotid artery, and to a Venturi effect in the aorta at the peak of aortic flow. Augmentation is systematically higher in the left ventricle than in the aorta, and systematically higher in the aorta than in more peripheral arteries such as the carotid or radial. Since properties of upper limb arteries are relatively constant with age, blood pressure, gender and drug therapy, a generalized transfer function can be used to synthesize the aortic from the radial pressure waveform. Comparison of measured directly and aortic pressure calculated with the SphygmoCor® process under control conditions and with nitroglycerine infusion gave values of augmentation with mean difference 0.9, SD 7.7 mmHg, which lie within AAMI criteria for equivalence, as do measures of end systolic pressure (difference 3.8, SD 3.6 mm Hg).

Rapid administration of a narcotic and neuromuscular blocker: a hemodynamic comparison of fentanyl, sufentanil, pancuronium, and vecuronium

High-dose narcotic anesthetic inductions usually avoid circulatory depression bettrthan do other techniques; however, the selection of a narcotic and neuromuscular blocker influences subsequent hemodynamic responses. One hundred-one patients having aortocoronary bypass graft (CABG) surgery were investigated using four combinations of a narcotic and neuromuscular blocker: group FP (fentanyl 50 μg/kg, pancuronium 100 μg/kg); group FV (fentanyl 50 μg/kg, vecuronium 80 μg/kg); group SP (sufentanil 10 μg/kg, pancuronium 100 μg/kg); and group SV (sufentanil 10 μg/kg, vecuronium 80 μg/kg), each combination being administered over 2 minutes. Hemodynamic functions were then monitored for 10 minutes before tracheal intubation. Significant changes included increases in heart rate in the groups receiving pancuronium and decreases in those receiving vecuronium. In all groups mean arterial pressure initially decreased; systemic vascular resistance index decreased significantly in all groups except SV. Cardiac index decreased significantly only in group SV. Circulatory depression requiring treatment with vasopressor or anticholinergic drugs was more common in patients given vecuronium. Cardiac arrhythmia occurred most often in group SP; only in group FP were there no arrhythmias, ischemic changes, or hemodynamic disturbances requiring intervention. Time to onset of neuromuscular blockade did not differ among the four groups, but transient chest wall rigidity occurred significantly more often with sufentanil than with fentanyl. Overall, the fentanyl/pancuronium combination afforded the greatest hemodynamic stability, whereas the sufentanil/vecuronium combination proved least satisfactory because of bradycardia and hypotension, requiring treatment in 35% of group SV patients. Differences in anesthetic premedication, social habits, preoperative medications, narcotic and muscle relaxant doses, and speed of anesthetic drug administration may also influence hemodynamicresponses and may explain differing results reported by others using the same drug combinations.

Radial Artery-to-Aorta Pressure Difference after Discontinuation of Cardiopulmonary Bypass

To test whether the radial artery-to-aorta pressure gradient seen in some patients after cardiopulmonary bypass (CPB) is due to reduction in hand vascular resistance, the authors compared pressures in the ascending aorta with pressures in the radial artery before and after CPB in 12 patients. They increased hand vascular resistance by briefly occluding the radial and ulnar arteries at the wrist and recorded that effect on the radial artery-to-aorta pressure relationship. They also recorded the effect of wrist compression on radial artery pressures before and after CPB in 38 patients not having aortic pressure measurements. Before CPB in the first 12 patients, the radial systolic arterial pressure (SAP) was significantly higher (P less than 0.05) than the ascending aortic SAP, and wrist compression did not significantly affect that difference (P greater than 0.05). After CPB, the radial artery and aortic SAPs were not statistically different (P greater than 0.05), but wrist compression restored the higher radial artery SAP. The mean arterial pressure (MAP) was equal in four patients and 1-3 mmHg higher or lower in eight patients before CPB, and wrist compression did not alter those relationships. After CPB, MAP was equal in four patients; radial MAP was 1-3 mmHg higher or lower in six patients, and 7 and 10 mmHg lower in the last two patients.(ABSTRACT TRUNCATED AT 250 WORDS)

A comparison of radial, brachial, and aortic pressures after cardiopulmonary bypass

Previous investigations have identified falsely low radial artery pressures after cardiopulmonary bypass (CPB). The present study investigates the relationship among radial, brachial, and aortic arterial pressures in 33 cardiac surgical patients following CPB. Two minutes after separation from CPB, clinically important (greater than or equal to 10 mmHg) underestimation of systolic aortic pressures occurred in 17 of 33 (52%) radial artery catheters, while occurring in seven of 33 (21%) brachial artery catheters. Radial artery mean pressure underestimated aortic mean pressure by greater than or equal to 5 mmHg in 21 of 33 (61%) patients two minutes after CPB, while an equivalent aortic-to-brachial artery mean arterial pressure difference occurred in nine of 33 (27%) patients. The incidence of aortic-to-radial mean arterial pressure differences greater than or equal to 5 mmHg decreased to 40% (four of ten patients) by ten minutes after CPB, although interpretation is complicated by decreased availability of aortic pressure measurements. Multivariate analysis failed to identify factors predisposed to central-to-peripheral pressure gradients. Radial and brachial arterial pressures were compared both before and after CPB in all 33 patients. Brachial artery systolic and mean pressures were higher than corresponding radial artery measurements two minutes after CPB (P less than 0.05), followed by gradual resumption of a normal brachial-to-radial pressure relationship over 60 minutes. Either vasospasm in the brachial and radial arteries or profound arteriolar vasodilation in the upper extremity might cause the observed central-to-peripheral arterial pressure differences. The progressive central-to-peripheral decrease in mean arterial pressure favors the latter mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)

Hemodynamic Effects of Intraaortic Administration of Protamine

Seventy-nine consecutive patients were given protamine rapidly into the ascending aorta during neutralization of heparin at the end of cardiopulmonary bypass. Simultaneously left atrial, diastolic pulmonary arterial, or right atrial pressures were maintained constant by appropriate infusion of oxygenated blood into the aorta. The systemic and pulmonary vascular resistances did not change, mean arterial blood pressure increased slightly, and cardiac output increased significantly (p less than 0.001). It seems that this method of heparin neutralization is safe provided that the intravascular volume can be maintained constant.

Pressure wave analysis is useful to understand the pathophysiology of preeclampsia, but perhaps not the rapid changes during cesarean delivery.

Pressure Wave Analysis Is Useful to Understand the Pathophysiology of Preeclampsia, but Perhaps Not the Rapid Changes during Cesarean Delivery IN this issue of ANESTHESIOLOGY, Dyer et al. tested the hypothesis that continuous monitoring of cardiac output (CO) in patients with severe preeclampsia during spinal anesthesia for cesarean delivery would give better information on the uteroplacental blood flow than mean radial artery blood pressure. They found that CO, as inferred from pressure wave analysis (PWA), did not decrease significantly from baseline if the mean radial artery blood pressure was maintained at baseline levels with intermittent vasoactive treatment, concluding that spinal anesthesia was associated with clinically insignificant changes in CO. The purposes of this editorial are to describe the contributions of PWA to our understanding physiologic changes during pregnancy and preeclampsia and to question whether PWA can be used to inform us of changes during cesarean delivery. Pressure wave analysis has been used as part of in-depth investigations of cardiovascular adaptations during pregnancy. Pressure and flow waves depend on the compliance of large and medium arteries, and vascular tone of arterioles and veins. A typical cardiac cycle is comprised of two pressure peaks, labeled P1 and P2 in order of timing. The decrease in arterial compliance with age has been related, by analysis of the aortic pressure and flow waves, to the progressive increase of P2 (augmentation), which overtakes the height of P1 (input impedance) at age 30 years. Poppas et al., assessing pulse pressure and flow, aortic flow velocities, and left ventricular (LV) imaging during the first, second, and third trimesters of normal pregnancy, found decreased aortic input impedance starting in the first trimester and decreased augmentation in the second and third trimesters; peripheral vascular resistance decreased moderately, and CO increased. Therefore, early pregnancy produces a temporary return of the arterial system aging to that seen in normal adolescents. Mesa et al. assessed LV function by echocardiography at the end of each trimester of normal pregnancy in 37 women. CO increased significantly, as did heart rate and stroke volume; peripheral vascular resistance decreased and LV wall thickness and mass increased from the second trimester to the end of pregnancy, thus indicating LV hypertrophy at the end of pregnancy, similar to that seen in long distance runners. Eduard et al. studied the role of the arterial and venous systems’ tone in the hemodynamic changes of normal pregnancy in the first and second trimesters and 3 months after delivery, using plethysmography, pulse wave velocity, and echocardiography. From the first trimester, heart rate and aortic distensibility increased, whereas systemic blood pressure and limb vascular resistance did not change. Lower limb venous tone increased from the first trimester, and their viscoelastic properties decreased in the third trimester, whereas no change occurred in the upper limbs. The LV diastolic diameter increased in the third trimester. These changes regressed 3 months after delivery. Therefore, the first cardiovascular change during pregnancy is the increase in arterial compliance, starting in the first trimester, with the appropriate conditioning in cardiac function to follow. Elvan-Taşpinar et al., using aortic PWA and pressure wave velocity, studied the effect of preeclampsia by assessment of aortic compliance in 51 normotensive women, 38 hypertensive women without proteinuria, and 33 preeclamptic women during the third trimester of pregnancy. Aortic impedance was significantly higher in preeclamptic and hypertensive than in normotensive patients. Ejection duration and aortic pulse pressure were significantly greater in preeclamptic than in normotensive and hypertensive patients, indicating that the vascular rigidity was severe enough to increase the LV ejection time and the pressure needed to eject each stroke volume. However, the subendocardial viability ratios were not significantly different among the three groups; hence, preeclampsia reversed the high arterial compliance of pregnancy but increased LV hypertrophy. Therefore, preeclampsia encompasses a severe decrease of vascular compliance and LV hypertrophy, plus the known decreased blood volume. Dyer et al. used the LiDCO device (LiDCO, London, United Kingdom) to examine rapid changes in cardiovascular variables associated with spinal anesthesia, vasopressor treatment, and oxytocin. However, this method of CO assessment is not recommended during hemodynamic instability and has been shown to produce CO assessment errors of greater than 33% during cardiac surgery. This method is based on the aortic PWA. Murgo et al. recorded flow and pressure waves from the aortic root, assessed their relation in their frequency domain, and then related the pattern of the impedance spectral plots to the analog shape of the pressure wave. The peak of flow aligned with P1, and the peak of the reflected pressure wave aligned with P2, which slows the flow wave without decreasing This Editorial View accompanies the following article: Dyer RA, Piercy JL, Reed AR, Lombard CJ, Schoeman LK, James MF: Hemodynamic changes associated with spinal anesthesia for cesarean delivery in severe preeclampsia. ANESTHESIOLOGY 2008; 108:802–11.

Predicting the pharmacodynamics of heparin: a clinical evaluation of the hepcon system 4

The magnitude of the anticoagulation response to heparin (heparin responsiveness) varies substantially from patient to patient. Identifying extremes of sensitivity and resistance prior to intravenous administration of heparin would facilitate anticoagulation for cardiopulmonary bypass (CPB). The performance of the Hepcon System 4 (HemoTec, Inc, Englewood, CO), an instrument designed for that purpose, was tested. Using nonheparinized blood samples from 157 patients scheduled for surgery requiring CPB, this device performed activated coagulation times (ACT) with three different concentrations of in vitro heparin. After determining each patients in vitro heparin response, the heparin dose predicted to produce ACT values of 480 seconds (group 1, N = 77) or 600 seconds (group 2, N = 80) was administered. Five minutes later each patients ACT was determined with the Hemochron method (International Technidyne, Inc, Edison, NJ). Simultaneously, several other variables that might predict heparin responsiveness were investigated. When compared with the observed ACT, the Hepcon System 4 inadequately predicted the response. There was considerable scatter in this comparison, but most frequently the in vitro method substantially underestimated the in vivo heparin dose requirement. Heparin responsiveness decreased significantly with high platelet counts and advanced age, but was unaffected by the initial hematocrit, ACT, partial thromboplastin time, or preoperative heparin therapy. Previous investigations have not identified a relationship between advanced age and reduced heparin responsiveness. Combining the Hepcon heparin dose-response in vitro method with the other parameters evaluated, stepwise regression could only account for 39% of the observed variability in heparin responsiveness.(ABSTRACT TRUNCATED AT 250 WORDS)

Systolic pressure measurement in the ascending aorta: Augmentation at the aortic cannula sideport

To assess whether arterial blood pressure measured at the sideport of the aortic cannula mirrors that measured within the ascending aorta, the two pressures were compared in 10 consecutive patients undergoing cardiopulmonary bypass. The mean arterial pressures (MAP) were equal both before and after bypass, but the sideport systolic arterial pressure (SAP) was 6.0 +/- 0.8 mm Hg higher than the aortic SAP before bypass and 9.1 +/- 0.5 mm Hg higher than the aortic SAP after bypass (P less than 0.001). Hematocrit, blood temperature, cardiac output, and heart rate did not correlate with the differences in SAP, suggesting that the higher SAP seen at the sideport was generated within the tube connecting the oxygenator to the aorta. This theory was investigated by decreasing the tube length distal to the sideport in three patients in this group who had sideport SAPs higher than their aortic SAPs, a measure that decreased the SAP difference between the two sites. At the end of cardiopulmonary bypass in 20 other consecutive patients, the effect of shortening the aorta-oxygenator tube from 1.8 to 0.25 m was tested. The SAP in the sideport decreased by 4 to 12 mm Hg in 12 of the 20 patients, while the MAP was unaffected by this maneuver. It is concluded that the MAP measured at the sideport of the aortic cannula closely reflects the MAP in the ascending aorta, whereas the SAP measured at the sideport does not reflect the aortic SAP. Thus, when aortic pressure is measured at the sideport to confirm an artificially low radial arterial pressure, systolic amplification at the sideport might simulate or exaggerate radial artery hypotension.